The objective of this study is to clarify the relationship between oxygen tension, metabolic activity and atheromatosis in the arterial wall. While most reports agree that artery metabolism undergoes some change before as well as during atherogenesis, there is no unanimity as to the role of PO2 and whether OO2 increases or decreases. Knowledge of the changes in energy pattern during atherogenesis should help our understanding of the mechanisms involved in the initiation of plaques and in their subsequent progression. Part of the confusion in the O2- atherosclerosis relationship may be the result of a lack of specificity in way the comparisions are carried out; this is usually between an overall O2 uptake measurement for an entire segment of artery and an overall subjective score for the range of disease normally present in that segment. Considering the focal nature of atherosclerosis and its tendency to localize in the intima, a more meaningful analysis should result from a point-by-point comparison between the oxygen measurements and lesion severity over the endothelial surface of the affected vessel. This will be accomplished by means of micro-O2 electrodes. To place the results of a point-by-point mapping of intimal PO2 into perspective, the study would include the more conventional measurements of average metabolic activity, average atherosclerotic involvement and average chemical composition of the respective arterial segments. The work will be done on the aortas of chickens with spontaneous lesions and also on aortas of rabbits with cholesterol induced lesions.